Tier 3 — preclinical

SIRT6 activation attenuates inflammatory-fibrogenic events, improves lung function and survival in experimental pulmonary fibrosis

Mousumi Ghosh, Nidhi Sharma, Siddhartha Moulik, Sai Balaji Andugulapati
Biochemical Pharmacology 2026 250(Pt 1):117940

Bibliography

PubMed
PMID 41916469
DOI
10.1016/j.bcp.2026.117940

Study snapshot

DesignCellular inflammation/fibrosis experiments plus bleomycin-induced pulmonary fibrosis in mice.
ModelRAW264.7 macrophages, human lung fibroblasts and bleomycin-treated mice.
Sample
InterventionMDL-800 SIRT6 activation; SIRT6 knockdown for mechanistic validation.
DurationModel-specific.
EndpointsInflammatory mediators; Fibrotic markers; Histone acetylation; NF-kB signaling; Lung compliance; Airway resistance; Survival

What the study showed, in plain terms

MDL-800 reduced inflammatory and fibrotic signaling in lung-cell models and improved fibrosis, lung mechanics and survival in bleomycin-treated mice. SIRT6 knockdown weakened the effect, supporting target dependence.

Key findings

MDL-800 produced SIRT6-dependent epigenetic and anti-fibrotic effects and improved lung-function measures in experimental pulmonary fibrosis.

What this study can and cannot tell us

The findings are preclinical and model-specific. Bleomycin fibrosis is not identical to idiopathic pulmonary fibrosis in humans, and MDL-800 has no established human IPF efficacy.

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability